Somatic Evolution in Non-neoplastic IBD-Affected Colon
Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. We whole-genome sequenced 446 colonic crypts from 46 IBD patients and compared these to 412 crypts from 41 non-IBD controls from our previous publication on the mutation lan...
Uloženo v:
| Vydáno v: | Cell Ročník 182; číslo 3; s. 672 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
06.08.2020
|
| Témata: | |
| ISSN: | 1097-4172, 1097-4172 |
| On-line přístup: | Zjistit podrobnosti o přístupu |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. We whole-genome sequenced 446 colonic crypts from 46 IBD patients and compared these to 412 crypts from 41 non-IBD controls from our previous publication on the mutation landscape of the normal colon. The average mutation rate of affected colonic epithelial cells is 2.4-fold that of healthy colon, and this increase is mostly driven by acceleration of mutational processes ubiquitously observed in normal colon. In contrast to the normal colon, where clonal expansions outside the confines of the crypt are rare, we observed widespread millimeter-scale clonal expansions. We discovered non-synonymous mutations in ARID1A, FBXW7, PIGR, ZC3H12A, and genes in the interleukin 17 and Toll-like receptor pathways, under positive selection in IBD. These results suggest distinct selection mechanisms in the colitis-affected colon and that somatic mutations potentially play a causal role in IBD pathogenesis. |
|---|---|
| AbstractList | Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. We whole-genome sequenced 446 colonic crypts from 46 IBD patients and compared these to 412 crypts from 41 non-IBD controls from our previous publication on the mutation landscape of the normal colon. The average mutation rate of affected colonic epithelial cells is 2.4-fold that of healthy colon, and this increase is mostly driven by acceleration of mutational processes ubiquitously observed in normal colon. In contrast to the normal colon, where clonal expansions outside the confines of the crypt are rare, we observed widespread millimeter-scale clonal expansions. We discovered non-synonymous mutations in ARID1A, FBXW7, PIGR, ZC3H12A, and genes in the interleukin 17 and Toll-like receptor pathways, under positive selection in IBD. These results suggest distinct selection mechanisms in the colitis-affected colon and that somatic mutations potentially play a causal role in IBD pathogenesis. Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. We whole-genome sequenced 446 colonic crypts from 46 IBD patients and compared these to 412 crypts from 41 non-IBD controls from our previous publication on the mutation landscape of the normal colon. The average mutation rate of affected colonic epithelial cells is 2.4-fold that of healthy colon, and this increase is mostly driven by acceleration of mutational processes ubiquitously observed in normal colon. In contrast to the normal colon, where clonal expansions outside the confines of the crypt are rare, we observed widespread millimeter-scale clonal expansions. We discovered non-synonymous mutations in ARID1A, FBXW7, PIGR, ZC3H12A, and genes in the interleukin 17 and Toll-like receptor pathways, under positive selection in IBD. These results suggest distinct selection mechanisms in the colitis-affected colon and that somatic mutations potentially play a causal role in IBD pathogenesis.Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. We whole-genome sequenced 446 colonic crypts from 46 IBD patients and compared these to 412 crypts from 41 non-IBD controls from our previous publication on the mutation landscape of the normal colon. The average mutation rate of affected colonic epithelial cells is 2.4-fold that of healthy colon, and this increase is mostly driven by acceleration of mutational processes ubiquitously observed in normal colon. In contrast to the normal colon, where clonal expansions outside the confines of the crypt are rare, we observed widespread millimeter-scale clonal expansions. We discovered non-synonymous mutations in ARID1A, FBXW7, PIGR, ZC3H12A, and genes in the interleukin 17 and Toll-like receptor pathways, under positive selection in IBD. These results suggest distinct selection mechanisms in the colitis-affected colon and that somatic mutations potentially play a causal role in IBD pathogenesis. |
| Author | Butler, Timothy Raine, Tim Strongili, Konstantina Hooks, Yvette Anderson, Carl A Tripathi, Monika Sanders, Mathijs A Jung, Hyunchul Stratton, Michael R Campbell, Peter J Lee-Six, Henry Arestang, Kenneth Olafsson, Sigurgeir McIntyre, Rebecca E Martincorena, Inigo Parkes, Miles Dawson, Claire Coorens, Tim Robinson, Philip S |
| Author_xml | – sequence: 1 givenname: Sigurgeir surname: Olafsson fullname: Olafsson, Sigurgeir organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 2 givenname: Rebecca E surname: McIntyre fullname: McIntyre, Rebecca E organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 3 givenname: Tim surname: Coorens fullname: Coorens, Tim organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 4 givenname: Timothy surname: Butler fullname: Butler, Timothy organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 5 givenname: Hyunchul surname: Jung fullname: Jung, Hyunchul organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 6 givenname: Philip S surname: Robinson fullname: Robinson, Philip S organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK; University of Cambridge, Department of Paediatrics, Cambridge CB2 0QQ, UK – sequence: 7 givenname: Henry surname: Lee-Six fullname: Lee-Six, Henry organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 8 givenname: Mathijs A surname: Sanders fullname: Sanders, Mathijs A organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK; Department of Hematology, Erasmus University Medical Center, Postbus 2040, 3000 CA Rotterdam, the Netherlands – sequence: 9 givenname: Kenneth surname: Arestang fullname: Arestang, Kenneth organization: Department of Gastroenterology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridgeshire CB2 0QQ, UK – sequence: 10 givenname: Claire surname: Dawson fullname: Dawson, Claire organization: Department of Gastroenterology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridgeshire CB2 0QQ, UK – sequence: 11 givenname: Monika surname: Tripathi fullname: Tripathi, Monika organization: Department of Histopathology, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridgeshire CB2 0QQ, UK – sequence: 12 givenname: Konstantina surname: Strongili fullname: Strongili, Konstantina organization: Department of Gastroenterology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridgeshire CB2 0QQ, UK – sequence: 13 givenname: Yvette surname: Hooks fullname: Hooks, Yvette organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 14 givenname: Michael R surname: Stratton fullname: Stratton, Michael R organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 15 givenname: Miles surname: Parkes fullname: Parkes, Miles organization: Department of Gastroenterology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridgeshire CB2 0QQ, UK – sequence: 16 givenname: Inigo surname: Martincorena fullname: Martincorena, Inigo organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 17 givenname: Tim surname: Raine fullname: Raine, Tim organization: Department of Gastroenterology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridgeshire CB2 0QQ, UK – sequence: 18 givenname: Peter J surname: Campbell fullname: Campbell, Peter J organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – sequence: 19 givenname: Carl A surname: Anderson fullname: Anderson, Carl A email: carl.anderson@sanger.ac.uk organization: Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK. Electronic address: carl.anderson@sanger.ac.uk |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32697969$$D View this record in MEDLINE/PubMed |
| BookMark | eNpNj01LxDAYhIOsuB_6BzxIj15a36RN0hzXddWFRQ_quSTpW-jSJrVpBf-9XVzB0wzMwzCzJDPnHRJyTSGhQMXdIbHYNAkDBgmIBFJxRhYUlIwzKtnsn5-TZQgHAMg55xdknjKhpBJqQcSbb_VQ22j75ZtxqL2Lahe9eBc79F2jwzHb3T_E66pCO2AZbXzj3SU5r3QT8OqkK_LxuH3fPMf716fdZr2PLefZEJfaQKq4qnLKwWibAsVMSD1NyrTkFnOrUGnKqcmRSyVZyg2UJgdpSlEiW5Hb396u958jhqFo63B8rad5YyhYxgRPhVDZhN6c0NG0WBZdX7e6_y7-vrIfPQ1XUQ |
| CitedBy_id | crossref_primary_10_1038_s41568_025_00868_x crossref_primary_10_1172_JCI191855 crossref_primary_10_1016_j_tcb_2021_07_002 crossref_primary_10_1093_intimm_dxac059 crossref_primary_10_1038_s41598_023_34631_9 crossref_primary_10_1146_annurev_cancerbio_061421_012447 crossref_primary_10_1038_s41467_022_29920_2 crossref_primary_10_1073_pnas_2112704118 crossref_primary_10_1158_2159_8290_CD_22_0145 crossref_primary_10_7717_peerj_18347 crossref_primary_10_1093_ecco_jcc_jjab199 crossref_primary_10_1038_s41586_025_08708_6 crossref_primary_10_1146_annurev_cancerbio_070620_091632 crossref_primary_10_1038_s41580_022_00538_y crossref_primary_10_1186_s40001_023_01566_w crossref_primary_10_1038_s41588_024_01922_4 crossref_primary_10_1038_s41586_021_03477_4 crossref_primary_10_1038_s41588_021_00930_y crossref_primary_10_1126_science_abm5874 crossref_primary_10_1038_s12276_023_01140_8 crossref_primary_10_1172_jci_insight_188281 crossref_primary_10_3390_biomedicines8100414 crossref_primary_10_1093_ecco_jcc_jjad025 crossref_primary_10_1016_j_cell_2024_02_009 crossref_primary_10_1002_aac2_12061 crossref_primary_10_1038_s41586_021_03790_y crossref_primary_10_1038_s41467_022_35592_9 crossref_primary_10_3389_fcell_2021_706755 crossref_primary_10_1038_s41388_023_02802_7 crossref_primary_10_3389_fmed_2021_644333 crossref_primary_10_1136_jcp_2024_209601 crossref_primary_10_1073_pnas_2023373118 crossref_primary_10_3390_ijms241311217 crossref_primary_10_1093_pnasnexus_pgae472 crossref_primary_10_1056_NEJMe2030754 crossref_primary_10_3390_cancers16020374 crossref_primary_10_1038_s41596_020_00437_6 crossref_primary_10_1073_pnas_2019450117 crossref_primary_10_1038_s41586_021_03345_1 crossref_primary_10_1038_s41467_022_31341_0 crossref_primary_10_3390_cancers17020229 crossref_primary_10_1016_j_devcel_2020_11_010 crossref_primary_10_1038_s41568_021_00335_3 crossref_primary_10_1038_s41588_022_01296_5 crossref_primary_10_1038_s41591_025_03623_9 crossref_primary_10_1159_000527340 crossref_primary_10_1186_s13619_022_00143_6 crossref_primary_10_1016_j_stem_2023_05_012 crossref_primary_10_3390_jpm11020151 crossref_primary_10_1038_s41568_025_00838_3 crossref_primary_10_1016_j_devcel_2023_08_011 crossref_primary_10_1016_j_mrrev_2022_108426 crossref_primary_10_1126_science_abh1645 crossref_primary_10_1038_s41588_024_01755_1 crossref_primary_10_1038_s41586_021_03822_7 crossref_primary_10_1056_NEJMra2101920 crossref_primary_10_1146_annurev_physiol_061121_040048 crossref_primary_10_1016_j_tig_2021_06_012 crossref_primary_10_1038_s41431_022_01213_8 crossref_primary_10_1038_s41467_023_40608_z crossref_primary_10_1093_intimm_dxab048 crossref_primary_10_3389_fmolb_2024_1442611 crossref_primary_10_1016_j_ccell_2022_11_004 crossref_primary_10_3390_jcm13164815 crossref_primary_10_1016_j_ccell_2020_11_002 crossref_primary_10_1016_j_ccell_2023_11_003 crossref_primary_10_1038_s41385_022_00554_3 crossref_primary_10_1038_s41588_023_01537_1 crossref_primary_10_1038_s41598_023_41123_3 crossref_primary_10_1038_s41416_021_01273_5 crossref_primary_10_1038_s41467_024_53332_z crossref_primary_10_1038_s41586_025_09096_7 crossref_primary_10_1136_gutjnl_2025_335023 crossref_primary_10_3390_genes12111779 crossref_primary_10_3390_cells14080567 crossref_primary_10_1038_s41586_021_03836_1 crossref_primary_10_1038_s41568_022_00529_3 crossref_primary_10_1146_annurev_cancerbio_070620_094029 crossref_primary_10_1016_j_jpedsurg_2024_162116 crossref_primary_10_1016_j_jad_2025_120067 crossref_primary_10_4103_sjg_sjg_124_25 crossref_primary_10_1038_s44319_025_00373_0 crossref_primary_10_1002_aac2_12037 crossref_primary_10_1016_j_jaut_2022_102847 crossref_primary_10_1038_s41568_023_00648_5 crossref_primary_10_1080_1744666X_2023_2157262 crossref_primary_10_1016_j_neo_2021_03_010 crossref_primary_10_3389_fimmu_2023_1048598 crossref_primary_10_1038_s41588_023_01545_1 crossref_primary_10_1016_j_canlet_2024_216831 crossref_primary_10_1038_s12276_021_00680_1 crossref_primary_10_1093_intimm_dxaf020 crossref_primary_10_1038_s41467_022_33663_5 crossref_primary_10_1016_j_tim_2022_05_010 crossref_primary_10_1186_s13104_023_06333_y crossref_primary_10_1371_journal_pone_0276195 crossref_primary_10_3390_cancers17020219 crossref_primary_10_7759_cureus_82241 crossref_primary_10_1038_s43587_024_00589_0 crossref_primary_10_1038_s41389_023_00492_0 crossref_primary_10_1002_1878_0261_13275 crossref_primary_10_1093_stmcls_sxab020 crossref_primary_10_1038_s12276_022_00912_y crossref_primary_10_1136_svn_2022_001756 crossref_primary_10_1093_nar_gkab914 crossref_primary_10_1038_s41467_021_21675_6 crossref_primary_10_1038_s41467_022_28568_2 crossref_primary_10_1053_j_gastro_2021_04_042 crossref_primary_10_1016_j_gde_2021_05_005 crossref_primary_10_1038_s41586_024_08133_1 crossref_primary_10_1093_ecco_jcc_jjac101 crossref_primary_10_1111_acel_13613 crossref_primary_10_1038_s41392_024_01848_7 crossref_primary_10_1186_s13046_021_01920_y crossref_primary_10_1038_s41596_024_00962_8 crossref_primary_10_1016_j_isci_2024_110118 crossref_primary_10_1016_j_jaci_2024_05_008 crossref_primary_10_1165_rcmb_2020_0440TR crossref_primary_10_1007_s10689_025_00479_3 crossref_primary_10_3390_ijms22052284 crossref_primary_10_1007_s00428_025_04072_y crossref_primary_10_1007_s11357_024_01113_3 crossref_primary_10_3390_cancers13235915 crossref_primary_10_1007_s10620_020_06609_4 crossref_primary_10_1016_j_arr_2021_101316 crossref_primary_10_1016_j_semcdb_2022_09_006 crossref_primary_10_1126_science_abm3233 crossref_primary_10_3389_fbioe_2022_883791 crossref_primary_10_1161_JAHA_123_032483 crossref_primary_10_3389_fgene_2021_760039 crossref_primary_10_1146_annurev_immunol_101819_075147 |
| ContentType | Journal Article |
| Copyright | Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved. |
| Copyright_xml | – notice: Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved. |
| DBID | CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1016/j.cell.2020.06.036 |
| DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | no_fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1097-4172 |
| ExternalDocumentID | 32697969 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: Wellcome Trust grantid: 206194 – fundername: Cancer Research UK grantid: 21777 |
| GroupedDBID | --- --K -DZ -ET -~X 0R~ 0WA 1RT 1~5 29B 2FS 2WC 3EH 4.4 457 4G. 53G 5GY 5RE 62- 6J9 7-5 85S AAEDT AAEDW AAFWJ AAHBH AAKRW AAKUH AALRI AAMRU AAVLU AAXUO AAYWO ABCQX ABDGV ABJNI ABMAC ABOCM ACGFO ACGFS ACNCT ACVFH ADBBV ADCNI ADEZE ADVLN ADXHL AEFWE AENEX AEUPX AEXQZ AFPUW AFTJW AGCQF AGHSJ AGKMS AHHHB AIGII AITUG AKAPO AKBMS AKRWK AKYEP ALMA_UNASSIGNED_HOLDINGS AMRAJ APXCP ASPBG AVWKF AZFZN BAWUL CGR CS3 CUY CVF DIK DU5 E3Z EBS ECM EFKBS EIF F5P FCP FDB FIRID HH5 IH2 IHE IXB J1W JIG K-O KOO KQ8 L7B LX5 M3Z M41 N9A NPM O-L O9- OK1 P2P RNS ROL RPZ SCP SDG SDP SES SSZ TAE TN5 TR2 TWZ UKR UPT WH7 YZZ ZCA 7X8 |
| ID | FETCH-LOGICAL-c554t-dab03959f8150bac301e467a1724a75ce8c9e9a151b8e5797235b0db807bd6de2 |
| IEDL.DBID | 7X8 |
| ISICitedReferencesCount | 147 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000558649000013&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1097-4172 |
| IngestDate | Sat Sep 27 18:53:57 EDT 2025 Mon Jul 21 06:06:38 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 3 |
| Keywords | somatic mutations PIGR mutational signatures ZC3H12A Crohn's disease mutation rate ulcerative colitis IL17 intestinal epithelia inflammatory bowel disease |
| Language | English |
| License | Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c554t-dab03959f8150bac301e467a1724a75ce8c9e9a151b8e5797235b0db807bd6de2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://pubmed.ncbi.nlm.nih.gov/PMC7427325 |
| PMID | 32697969 |
| PQID | 2426536694 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_2426536694 pubmed_primary_32697969 |
| PublicationCentury | 2000 |
| PublicationDate | 2020-08-06 |
| PublicationDateYYYYMMDD | 2020-08-06 |
| PublicationDate_xml | – month: 08 year: 2020 text: 2020-08-06 day: 06 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Cell |
| PublicationTitleAlternate | Cell |
| PublicationYear | 2020 |
| SSID | ssj0008555 |
| Score | 2.649897 |
| Snippet | Inflammatory bowel disease (IBD) is a chronic inflammatory disease associated with increased risk of gastrointestinal cancers. We whole-genome sequenced 446... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | 672 |
| SubjectTerms | Adult Aged Aged, 80 and over Aging - genetics Clonal Evolution - genetics Clonal Evolution - immunology Colitis - genetics Colitis - metabolism Colitis, Ulcerative - genetics Colitis, Ulcerative - metabolism Crohn Disease - genetics Crohn Disease - metabolism DNA-Binding Proteins - genetics Epithelial Cells - metabolism Epithelial Cells - pathology F-Box-WD Repeat-Containing Protein 7 - genetics Female Humans INDEL Mutation Inflammatory Bowel Diseases - genetics Inflammatory Bowel Diseases - immunology Inflammatory Bowel Diseases - metabolism Inflammatory Bowel Diseases - pathology Interleukin-17 - metabolism Intestinal Mucosa - metabolism Intestinal Mucosa - pathology Male Middle Aged Mutation Rate Phylogeny Point Mutation Receptors, Cell Surface - genetics Ribonucleases - genetics Toll-Like Receptors - genetics Transcription Factors - genetics Whole Genome Sequencing |
| Title | Somatic Evolution in Non-neoplastic IBD-Affected Colon |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/32697969 https://www.proquest.com/docview/2426536694 |
| Volume | 182 |
| WOSCitedRecordID | wos000558649000013&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3NS8MwFH-oU_Di93R-UcFrsC5tmpxkzg0FLQMVditJ8wq7tNPNgf-9L2nHToLgpeTQQHh5X3n55f0Ari23t6G2DiplkUVYkM1hIWiE1lD873LrHwo_J2kqx2M1agpuswZWufSJ3lHbKnc18hsXSmIuhIruph_MsUa529WGQmMdWpxSGafVyXjVLVzGnvXUXbKyiCJ182imxne5wjidD7uh79_Jxe8ppg81w93_LnIPdpokM-jVWrEPa1gewFZNO_l9COK18o1ag8GiUbxgUgZpVbLS4cm1a90cPN0_sJ4He6AN-jSzPIL34eCt_8ga_gSWU5IwZ1abkKtYFZKyPqNzsmUkv6hJEpFO4hxlrlBpivlGYpw4_rHYhNbIMDFWWOy2YaOsSjyBwJ3UtEQVaWEjHkmdKBMj_YVaFIaHHbhaCiQj_XSy1bTkr1m2EkkHjmupZtO6kUZGqaNKlFCnf5h9Bttuszz2TpxDqyDrxAvYzBfzyezz0m88fdPRyw-eyLcF |
| linkProvider | ProQuest |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Somatic+Evolution+in+Non-neoplastic+IBD-Affected+Colon&rft.jtitle=Cell&rft.au=Olafsson%2C+Sigurgeir&rft.au=McIntyre%2C+Rebecca+E&rft.au=Coorens%2C+Tim&rft.au=Butler%2C+Timothy&rft.date=2020-08-06&rft.issn=1097-4172&rft.eissn=1097-4172&rft.volume=182&rft.issue=3&rft.spage=672&rft_id=info:doi/10.1016%2Fj.cell.2020.06.036&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1097-4172&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1097-4172&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1097-4172&client=summon |